Hypertension, Vol 14, 396-403, Copyright © 1989 by American Heart Association
FC Luft, CS Wilcox, T Unger, R Kuhn, G Demmert, P Rohmeiss, D Ganten and RB Sterzel
To elucidate mechanisms of angiotensin II (Ang II)-related hypertension, we
infused angiotensin (76 ng/min s.c.) into rats with minipumps for 10-14
days. Control rats received sham pumps. We measured blood pressure by
tail-cuff, and the excretion of aldosterone and prostaglandins (PG) (PGE2,
prostacyclin derivative 6kPGF1 alpha, and thromboxane [Tx] derivative
TxB2). Angiotensin II increased blood pressure by 20 mm Hg by day 2 and by
90 mm Hg by day 10. Aldosterone excretion increased from 10 to 70 ng/day in
Ang II rats by day 7. Urine PGE2 did not increase in angiotensin rats;
however, both 6kPGF1 alpha and TxB2 excretion increased with angiotensin.
Control rats had no changes in any of these parameters. A sympathetic
component was tested in a separate group of angiotensin rats that received
phenoxybenzamine (300 micrograms/kg/day) during angiotensin infusion; their
increase in blood pressure of 40 mm Hg at 10 days was less than in those
rats with angiotensin alone but more than in control rats. Phenoxybenzamine
did not influence the angiotensin-induced increases in excretion of 6kPGF1
alpha or TxB2. Additional groups of conscious angiotensin and control rats
were equipped with splanchnic nerve electrodes on day 14 for recording of
sympathetic nerve activity. Angiotensin rats had greater basal sympathetic
nerve activity than the control rats. Incremental methoxamine injections
demonstrated altered baroreceptor reflex function in rats receiving
angiotensin. We conclude that increased blood pressure with chronic
angiotensin infusion is accompanied by increased production of aldosterone
and increased sympathetic tone. The latter may be modulated by PG.
ARTICLES
Angiotensin-induced hypertension in the rat. Sympathetic nerve activity and prostaglandins
Department of Physiology, University of Heidelberg, FRG.
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